In vitro effects of non-steroidal anti-inflammatory drugs (Meloxicam and Flunixin Meglumine) and phytochemical (Harpagoside) on the respiratory burst of porcine polymorphonuclear neutrophils (PMNs)

Author(s):  
Giuseppe Marruchella ◽  
Francesco Mosca ◽  
Jasmine Hattab ◽  
Abigail R. Trachtman ◽  
Pietro G. Tiscar

Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used in veterinary medicine. Additionally, interest regarding the anti-infammatory properties of phytochemicals has emerged in recent years. In the present study, we aim to investigate the in vitro effects of meloxicam, flunixin meglumine, and harpagoside on the respiratory burst of porcine polymorphonuclear neutrophils (PMNs). We observed that harpagoside was able to suppress the respiratory burst, similarly to flunixin meglumine. Conversely, meloxicam enhanced the PMNs response. However, these effects were only detected at concentrations higher than those achievable in plasma and tissues. The present study intends to offer insights into the role of these molecules on phagocytosis mechanisms in animals to complement what is already known regarding human PMNs.

Author(s):  
Asmaa Nabil-Adam ◽  
Mohamed A. Shreadah

Background: This study aimed to investigate the potential bioactivity and the ameliorative role of Galaxaura oblongata (G. oblongata) against LPS-induced toxicity by using hematological parameters. Objective: It is aimed also to examine its protective effect using the immunohistochemistry of liver and lungs as biomarkers in male BALB/C albino mice. Materials and Methods: the current study carried out using different in-vitro and in-vivo assays such as phytochemical, antioxidants, anti-inflammatory for in-vitro where the hematological and immunohistochemistry for lung and liver were investigated in vivo. Results: There are no previous studies were performed to investigate the in vivo and in vitro effects of the G. oblongata extracts as antioxidant and anti-inflammatory due to their rareness compared to other red algae. LPS treated mice revealed a significant decrease in total number of WBCs, RBCs, platelets, and HGB%, MPV, MCV and MCHC compared to the control group. On contrast, the HCT and MCHC were increased in the induction group which was treated with LPS compared to the control group. Furthermore, the immunohistochemistry results of the present study revealed the protective effect of G. oblongata compared to the induction group. G. oblongata can be used as protective marine natural products against the toxicity induced by LPS. Conclusion: It exhibited a significant ameliorative role against the alterations in the hematological parameters and immunohistochemistry of liver and lungs, and helps to reduce as well as coordinate the acute inflammations caused by TNF.


Drugs in R&D ◽  
2004 ◽  
Vol 5 (6) ◽  
pp. 327-330 ◽  
Author(s):  
S??kr?? ??zt??rk ◽  
Banu G K??seoglu ◽  
H??lya Ko??ak ◽  
S??kr?? Palanduz ◽  
Kivan?? ??efle ◽  
...  

1978 ◽  
Vol 40 (01) ◽  
pp. 024-036 ◽  
Author(s):  
William Diamantis ◽  
William C Kohlhepp ◽  
Barbara Haertlein ◽  
John Melton ◽  
R Duane Sofia

SummaryMeseclazone and its major metabolite, 5-chlorosalicylic acid (5-CSA) have been shown to possess anti-inflammatory, analgesic and antipyretic activity. The comparative effects of these compounds on platelet aggregation were evaluated in vitro and ex vitro with acetylsalicylic acid (ASA). in vitro, meseclazone and ASA exhibited almost identical inhibitory potency of secondary phase ADP aggregation while 5-CSA was less effective. Moreover, collagen aggregation was inhibited by all three agents: ASA > meseclazone > 5- CSA. Thrombin-induced aggregation was inhibited to approximately the same extent by 5- CSA and ASA while meseclazone was inactive. The in vitro effects on the release-inducing aggregants were confirmed by ex vitro experiments in rats. These demonstrated that ASA and meseclazone inhibited collagen-induced aggregation 1 and 4 hr after oral administration although ASA was three to four times more active. ASA, but not meseclazone, was still effective 24 hr after administration. Bleeding times in rats 1 and 4 hr following oral administration of meseclazone and ASA were not altered. It is concluded that meseclazone and/or 5-CSA inhibit in vitro and ex vitro platelet aggregation initiated by the release reaction similar to ASA and other non-steroidal anti-inflammatory drugs.


2018 ◽  
Vol 11 (4) ◽  
pp. 330-346 ◽  
Author(s):  
João Alfredo Moraes ◽  
Ana Clara Frony ◽  
Pedro Barcellos-de-Souza ◽  
Marcel Menezes da Cunha ◽  
Thayanne Brasil Barbosa Calcia ◽  
...  

Exposition of neutrophils (polymorphonuclear neutrophils, PMNs) to bacterial products triggers exacerbated activation of these cells, increasing their harmful effects on host tissues. We evaluated the possibility of interfering with the classic immune innate responses of human PMNs exposed to bacterial endotoxin (lipopolysaccharide, LPS), and further stimulated with bacterial formyl peptide (N-formyl-methionine-leucine-phenylalanine, fMLP). We showed that the low- molecular-weight fucoidan (LMW-Fuc), a polysaccharide extracted from brown algae, attenuated the exacerbated activation induced by fMLP on LPS-primed PMNs, in vitro, impairing chemotaxis, NET formation, and the pro-survival and pro-oxidative effects. LMW-Fuc also inhibited the activation of canonical signaling pathways, AKT, bad, p47phox and MLC, activated by the exposition of PMN to bacterial products. The activation of PMN by sequential exposure to LPS and fMLP induced the release of L-selectin+ microparticles, which were able to trigger extracellular reactive oxygen species production by fresh PMNs and macrophages. Furthermore, we observed that LMW-Fuc inhibited microparticle release from activated PMN. In vivo experiments showed that circulating PMN-derived microparticles could be detected in mice exposed to bacterial products (LPS/fMLP), being downregulated in animals treated with LMW-Fuc. The data highlight the autocrine and paracrine role of pro-inflammatory microparticles derived from activated PMN and demonstrate the anti-inflammatory effects of LMW-Fuc on these cells.


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